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Multiple mediators of adaptation are involved and interconnected in nonlinear networks [7]. When chronically stressed, the biphasic effects of numerous biomarkers eventually lead to AL and disease in a tripartite sequence: (1) overactivation of primary mediators such as stress hormones and pro-and anti-inflammatory cytokines induce primary effects on cellular activities; (2) subsequent secondary outcomes, whereby metabolic, cardiovascular, and second-order immune biomarkers become dysregulated, and (3) culmination in tertiary outcomes or clinical endpoints [7].

The AL model proposes that, by measuring the multisystemic, reciprocal interactions among primary mediators, primary effects, and secondary outcomes, individuals at a high risk for tertiary outcomes can be identified [8]. Physicians already routinely incorporate many related biomarkers in typical blood work, although attention is primarily placed on values reaching clinically significant levels. By including additional biomarkers, identifying preclinical values, and triangulating methods with interdisciplinary measures (e.g. genetic assessment, neuropsychological testing, clinical interviews, psychometrics, etc.), advances in diagnostic, treatment, and prevention strategies could be improved.